The choice of gut decontamination
procedure depends on the toxin and the circumstances
Observation of the Patient
Asymptomatic or mildly symptomatic patients should be observed for at least 4–6
hours. Longer observation is indicated if the ingested substance is a
sustained-release preparation or is known to slow gastrointestinal motility or
if there may have been exposure to a poison with delayed onset of symptoms
(such as acetaminophen, colchicine, or hepatotoxic mushrooms). After that time,
the patient may be discharged if no symptoms have developed and adequate
gastric decontamination has been provided. Before discharge, psychiatric
evaluation should be performed to assess suicidal risk. Intentional ingestions
in adolescents should raise the possibility of unwanted pregnancy or sexual
abuse.
The Symptomatic Patient
In symptomatic patients, treatment of life-threatening complications takes precedence over in-depth diagnostic evaluation. Patients with mild symptoms may deteriorate rapidly, which is why all potentially significant exposures should be observed in an acute care facility. The following complications may occur, depending on the type of poisoning.
Coma and gut decontamination
Coma is commonly associated with ingestion of large doses of antihistamines, benzodiazepines and other sedative-hypnotic drugs, -hydroxybutyrate (GHB), ethanol, opioids, antipsychotic drugs, or antidepressants. The most common cause of death in comatose patients is respiratory failure, which may occur abruptly. Pulmonary aspiration of gastric contents may also occur, especially in victims who are deeply obtunded or convulsing. Hypoxia and hypoventilation may cause or aggravate hypotension, arrhythmias, and seizures. Thus, protection of the airway and assisted ventilation are the most important treatment measures for any poisoned patient.
In symptomatic patients, treatment of life-threatening complications takes precedence over in-depth diagnostic evaluation. Patients with mild symptoms may deteriorate rapidly, which is why all potentially significant exposures should be observed in an acute care facility. The following complications may occur, depending on the type of poisoning.
Coma and gut decontamination
Coma is commonly associated with ingestion of large doses of antihistamines, benzodiazepines and other sedative-hypnotic drugs, -hydroxybutyrate (GHB), ethanol, opioids, antipsychotic drugs, or antidepressants. The most common cause of death in comatose patients is respiratory failure, which may occur abruptly. Pulmonary aspiration of gastric contents may also occur, especially in victims who are deeply obtunded or convulsing. Hypoxia and hypoventilation may cause or aggravate hypotension, arrhythmias, and seizures. Thus, protection of the airway and assisted ventilation are the most important treatment measures for any poisoned patient.
Treatment
of Gut Contamination
The initial emergency management of
coma can be remembered by the mnemonic ABCD, for Airway, Breathing,
Circulation, and Drugs (dextrose, thiamine, and naloxone or flumazenil),
respectively.
Airway
Establish a patent airway by positioning, suction, or insertion of an artificial nasal or oropharyngeal airway. If the patient is deeply comatose or if there is no gag or cough reflex, perform endotracheal intubation. These airway interventions may not be necessary if the patient is intoxicated by an opioid or a benzodiazepine and responds rapidly to intravenous naloxone or flumazenil (see below).
Establish a patent airway by positioning, suction, or insertion of an artificial nasal or oropharyngeal airway. If the patient is deeply comatose or if there is no gag or cough reflex, perform endotracheal intubation. These airway interventions may not be necessary if the patient is intoxicated by an opioid or a benzodiazepine and responds rapidly to intravenous naloxone or flumazenil (see below).
Breathing
Clinically assess the quality and depth of respiration, and provide assistance if necessary with a bag-valve-mask device or mechanical ventilator. Provide supplemental oxygen. The arterial blood CO2 tension is useful in determining the adequacy of ventilation. The arterial blood PO2 determination may reveal hypoxemia, which may be caused by respiratory arrest, bronchospasm, pulmonary aspiration, or noncardiogenic pulmonary edema. Pulse oximetry provides an assessment of oxygenation but is not reliable in patients with methemoglobinemia or carbon monoxide poisoning.
Circulation
Measure the pulse and blood pressure and estimate tissue perfusion (eg, by measurement of urinary output, skin signs, arterial blood pH). Place the patient on continuous ECG monitoring. Insert an intravenous line, and draw blood for glucose, electrolytes, serum creatinine and liver tests, and possible quantitative toxicologic testing.
Clinically assess the quality and depth of respiration, and provide assistance if necessary with a bag-valve-mask device or mechanical ventilator. Provide supplemental oxygen. The arterial blood CO2 tension is useful in determining the adequacy of ventilation. The arterial blood PO2 determination may reveal hypoxemia, which may be caused by respiratory arrest, bronchospasm, pulmonary aspiration, or noncardiogenic pulmonary edema. Pulse oximetry provides an assessment of oxygenation but is not reliable in patients with methemoglobinemia or carbon monoxide poisoning.
Circulation
Measure the pulse and blood pressure and estimate tissue perfusion (eg, by measurement of urinary output, skin signs, arterial blood pH). Place the patient on continuous ECG monitoring. Insert an intravenous line, and draw blood for glucose, electrolytes, serum creatinine and liver tests, and possible quantitative toxicologic testing.
Drugs
in Gut Decontamination
Dextrose and thiamine
Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50%dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.
Narcotic antagonists
Naloxone, 0.4–2 mg intravenously, may reverse opioid-induced respiratory depression and coma. It is often given empirically to any comatose patient with depressed respirations. If opioid overdose is strongly suspected, give additional doses of naloxone (up to 5–10 mg may be required to reverse the effects of potent opioids or propoxyphene). Note: Naloxone has a much shorter duration of action (2–3 hours) than most common opioids; repeated doses may be required, and continuous observation for at least 3–4 hours after the last dose is mandatory. Nalmefene, a newer opioid antagonist, has a duration of effect longer than that of naloxone but still shorter than that of the opioid methadone.
Gut Decontamination and Flumazenil
Flumazenil, 0.2–0.5 mg intravenously, repeated every 30 seconds as needed up to a maximum of 3 mg, may reverse benzodiazepine-induced coma. Caution: Flumazenil should not be given if the patient has coingested a tricyclic antidepressant, is a user of high-dose benzodiazepines, or has a seizure disorder because its use in these circumstances may precipitate seizures. In most circumstances, use of flumazenil is not advised as the potential risks outweigh its benefits. Note: Flumazenil has a short duration of effect (2–3 hours), and resedation requiring additional doses is common.
Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50%dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.
Narcotic antagonists
Naloxone, 0.4–2 mg intravenously, may reverse opioid-induced respiratory depression and coma. It is often given empirically to any comatose patient with depressed respirations. If opioid overdose is strongly suspected, give additional doses of naloxone (up to 5–10 mg may be required to reverse the effects of potent opioids or propoxyphene). Note: Naloxone has a much shorter duration of action (2–3 hours) than most common opioids; repeated doses may be required, and continuous observation for at least 3–4 hours after the last dose is mandatory. Nalmefene, a newer opioid antagonist, has a duration of effect longer than that of naloxone but still shorter than that of the opioid methadone.
Gut Decontamination and Flumazenil
Flumazenil, 0.2–0.5 mg intravenously, repeated every 30 seconds as needed up to a maximum of 3 mg, may reverse benzodiazepine-induced coma. Caution: Flumazenil should not be given if the patient has coingested a tricyclic antidepressant, is a user of high-dose benzodiazepines, or has a seizure disorder because its use in these circumstances may precipitate seizures. In most circumstances, use of flumazenil is not advised as the potential risks outweigh its benefits. Note: Flumazenil has a short duration of effect (2–3 hours), and resedation requiring additional doses is common.
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